Melatonin receptor-dependent antiarrhythmic action in rat in vivo model of heart post-ischemic reperfusion

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68407700%3A21460%2F23%3A00371881" target="_blank" >RIV/68407700:21460/23:00371881 - isvavai.cz</a>

Výsledek na webu

<a href="https://onlinelibrary.wiley.com/doi/10.1111/apha.14044" target="_blank" >https://onlinelibrary.wiley.com/doi/10.1111/apha.14044</a>

DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Melatonin receptor-dependent antiarrhythmic action in rat in vivo model of heart post-ischemic reperfusion

Popis výsledku v původním jazyce

Introduction: Melatonin has been proven to have cardioprotective effects most likely through promoted expression of antioxidant enzymes and suppression of inflammation-related genes. Hence, this study aimed to explore receptor-dependent pathways responsible for the melatonin antiarrhythmic action in a rat model of post-ischemic heart reperfusion (Wistar male rats n = 86, 3-month-old). Methods: Ischemia was induced by the left coronary artery ligation for 5 min. Melatonin (4 mg/kg, i.v.), luzindole (blocker of melatonin receptors, 0.4 mg/kg, i.v.), and a combination of melatonin + luzindole were infused before reperfusion and in the baseline. Incidence of ventricular fibrillation (VF) and conduction velocity were measured in vivo. Left ventricular tissue was used for expression of electrical coupling protein, connexin-43 (Cx43) and markers of oxidative stress evaluation. Results: Melatonin prevented ischemia-related conduction slowing and decreased VF incidence that was associated with increased myocardial phosphorylated (P) Cx43 abundance. Luzindole abolished melatonin antiarrhythmic effect, down-regulated Cx43 and protein kinase Cε that phosphorylates Cx43. However, melatonin did not change oxidative stress markers. Conclusion: We can assume, that the antiarrhythmic effect of melatonin was mediated by the improved conduction properties associated with enhanced Cx43 phosphorylation, most likely independent from its antioxidant effect.

Název v anglickém jazyce

Melatonin receptor-dependent antiarrhythmic action in rat in vivo model of heart post-ischemic reperfusion

Popis výsledku anglicky

Introduction: Melatonin has been proven to have cardioprotective effects most likely through promoted expression of antioxidant enzymes and suppression of inflammation-related genes. Hence, this study aimed to explore receptor-dependent pathways responsible for the melatonin antiarrhythmic action in a rat model of post-ischemic heart reperfusion (Wistar male rats n = 86, 3-month-old). Methods: Ischemia was induced by the left coronary artery ligation for 5 min. Melatonin (4 mg/kg, i.v.), luzindole (blocker of melatonin receptors, 0.4 mg/kg, i.v.), and a combination of melatonin + luzindole were infused before reperfusion and in the baseline. Incidence of ventricular fibrillation (VF) and conduction velocity were measured in vivo. Left ventricular tissue was used for expression of electrical coupling protein, connexin-43 (Cx43) and markers of oxidative stress evaluation. Results: Melatonin prevented ischemia-related conduction slowing and decreased VF incidence that was associated with increased myocardial phosphorylated (P) Cx43 abundance. Luzindole abolished melatonin antiarrhythmic effect, down-regulated Cx43 and protein kinase Cε that phosphorylates Cx43. However, melatonin did not change oxidative stress markers. Conclusion: We can assume, that the antiarrhythmic effect of melatonin was mediated by the improved conduction properties associated with enhanced Cx43 phosphorylation, most likely independent from its antioxidant effect.

Druh

O - Ostatní výsledky

CEP obor

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OECD FORD obor

30109 - Pathology

Projekt

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Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2023

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů